McCormack J, Gelband H, Xu H, Villafane J, Stolfi A, Pickoff A S
Department of Pediatrics, University of Miami School of Medicine, Florida 33101.
Pediatr Res. 1988 Jan;23(1):99-103. doi: 10.1203/00006450-198801000-00022.
Previous studies have suggested that the atrioventricular nodal functional refractory period in the neonate is equal to or shorter than that of the ventricle, providing little or no protection to the ventricle against rapid atrial rates and allowing closely coupled atrial beats to fall within the ventricular vulnerable period. We evaluated atrioventricular node function in 21 mongrel neonatal puppies, 3-15 days old, and 15 adult dogs utilizing intracardiac His bundle recording and stimulation techniques. The mean atrioventricular nodal functional refractory period (173.1 +/- 20.0 ms) exceeded both the ventricular effective refractory period (139.5 +/- 14.3) and ventricular functional refractory period (163.3 +/- 14.5) in the neonates. Furthermore, the atrioventricular node was the site of limiting antegrade conduction in all neonates. No ventricular arrhythmias were induced by atrial extrastimulation in any of the neonates. The site of conduction delay during atrial extrastimulation was confined to the atrioventricular node in 15/16 neonates (94%) while 1/16 (6%) had combined nodal and infranodal delay. The neonates developed Wenckebach, at significantly faster heart rates than the adults, but both groups developed Wenckebach at approximately twice the resting heart rate. Retrograde conduction was a consistent finding in the neonates. However, antegrade Wenckebach occurred at a significantly faster heart rate than retrograde Wenckebach suggesting different functional properties. Our data suggest that in the neonatal canine, the atrioventricular node functional refractory period is longer than both the ventricular effective refractory period and ventricular functional refractory period. Furthermore, the degree of protection offered by the neonatal atrioventricular node to the ventricle appears to be comparable to that of the adult.
先前的研究表明，新生儿的房室结功能不应期等于或短于心室的功能不应期，这对心室抵御快速心房率几乎没有或根本没有保护作用，使得紧密耦合的心房搏动落入心室易损期。我们利用心内希氏束记录和刺激技术，评估了21只3至15日龄的杂种新生幼犬和15只成年犬的房室结功能。新生儿的平均房室结功能不应期（173.1±20.0毫秒）超过了心室有效不应期（139.5±14.3）和心室功能不应期（163.3±14.5）。此外，在所有新生儿中，房室结是限制前向传导的部位。在任何新生儿中，心房额外刺激均未诱发室性心律失常。在16只新生儿中的15只（94%）中，心房额外刺激期间的传导延迟部位局限于房室结，而1/16（6%）有房室结和结下延迟并存。新生儿出现文氏现象时的心率明显快于成年犬，但两组出现文氏现象时的心率均约为静息心率的两倍。逆行传导在新生儿中是一个常见的发现。然而，前向文氏现象出现时的心率明显快于逆行文氏现象，提示两者具有不同的功能特性。我们的数据表明，在新生犬中，房室结功能不应期长于心室有效不应期和心室功能不应期。此外，新生儿房室结对心室的保护程度似乎与成年犬相当。
